PS Synthesis Study Ties Phospholipid Balance to ER Calcium Release

연구 결과는

Researchers from Wuhan University's Taikang School of Basic Medical Sciences and collaborators published the paper 'Phosphatidylserine synthesis tunes IP3R-mediated ER Ca2+ release via phospholipid homeostasis' in Cell Reports in August 2026.

In fruit flies, phosphatidylserine (PS) synthesis defects led to mitochondrial calcium overload and mitochondrial damage, and reducing IP3 receptor-mediated calcium release from the endoplasmic reticulum reversed those defects. In mammalian cells, both PS deficiency and excess PS production caused abnormal IP3R-mediated calcium release: deficiency produced sustained oscillatory calcium signals, while excess PS reduced the amplitude of calcium release.

Why Phospholipid Balance Matters

The team found that correcting phospholipid composition through the PE-SREBP axis in flies or the PC-SREBP axis in mammalian cells restored normal IP3R-mediated calcium release, leading the authors to conclude that phospholipid homeostasis imbalance is the root cause of the abnormal calcium signaling.

The study also connects PS metabolism to Lenz-Majewski syndrome, a rare condition associated with mutations that increase PS synthesis, and proposes the PS metabolism-IP3R-calcium homeostasis axis as a framework for understanding lipid-metabolism-related disorders.

구매자 요약

This is basic mechanism research rather than human efficacy evidence. For ingredient buyers, it is background science that helps explain why PS and other phospholipids attract continued academic interest, but it should not be used as claim support in supplement or food dossiers.

Nutranexa supplies phosphatidylserine ingredients and reports this study as research news without claiming any product-related outcome from it.

출처

• Cell Reports - Phosphatidylserine synthesis tunes IP3R-mediated ER Ca2+ release via phospholipid homeostasis
• Wuhan University - PS synthesis regulates ER calcium release mechanism